Calcium influx regulates antibody-induced glycoprotein movements within the Chlamydomonas flagellar membrane

1990 ◽  
Vol 96 (1) ◽  
pp. 27-33 ◽  
Author(s):  
R.A. Bloodgood ◽  
N.L. Salomonsky
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Gliding Motility ◽  
Free Calcium ◽  
Membrane Glycoprotein ◽  
Channel Blockers ◽  
Membrane Glycoproteins ◽  
Whole Cell ◽  
Flagellar Membrane

The Chlamydomonas flagellar surface exhibits a number of dynamic membrane phenomena associated with whole-cell gliding locomotion and the early events in fertilization. Crosslinking of a specific population of flagellar surface-exposed glycoproteins with the lectin concanavalin A or an anti-carbohydrate mouse monoclonal antibody, designated FMG-1, results in a characteristic pattern of glycoprotein redistribution within the plane of the flagellar membrane. Recent evidence suggests that flagellar membrane glycoprotein movements are associated with both whole-cell gliding motility and the early events in mating. It is of interest to determine the transmembrane signaling pathway whereby crosslinking of the external domains of flagellar glycoproteins activates the intraflagellar machinery responsible for translocation of flagellar membrane glycoproteins. The redistribution of flagellar membrane glycoproteins requires micromolar levels of free calcium in the medium; lowering the free calcium concentration to 10(−7) M results in complete but reversible inhibition of redistribution. Redistribution is maximal in the presence of 20 microM free calcium in the medium. Redistribution is inhibited in the presence of 20 microM free calcium by the calmodulin antagonists trifluoperazine, W-7 and calmidazolium, the calcium channel blockers diltiazem, methoxyverapamil (D-600) and barium chloride, and the local anesthetics, lidocaine and procaine. The actions of all of these agents can be interpreted in terms of a requirement for calcium in the signaling mechanism associated with flagellar glycoprotein redistribution. In particular, the requirement for micromolar calcium in the external medium and the effects of specific calcium channel blockers suggest that flagellar membrane glycoprotein crosslinking may induce an increase in calcium influx, which may be the initial trigger for activating the flagellar machinery responsible for active movement of flagellar membrane glycoproteins.

The Effect of Verapamil and Diltiazem on Alveolar Type II Cells during Warm and Cold Metabolic Ischaemia

1994 ◽  
Vol 22 (3) ◽  
pp. 153-159
Author(s):  
L Spaggiari ◽  
M Rusca ◽  
R Alfieri ◽  
P G Petronini ◽  
P Carbognani ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Total Protein Content ◽  
Free Calcium ◽  
Alveolar Type ◽  
Channel Blockers ◽  
Type Ii ◽  
Organ Protection ◽  
Cytosolic Free Calcium ◽  
Adult Rat

The alteration of cytosolic free calcium concentration is an important event during cellular ischaemia. Calcium channel blockers have been shown to be beneficial during experimental ischaemic organ protection. To investigate the mechanisms of this protection, the behaviour of type II pneumocyte cultures, subjected to warm and cold metabolic ischaemia (6 h), was studied. The cells were incubated in electrolytic solutions and treated with high doses of verapamil (10 mg/l) or diltiazem (100 mg/l). Alveolar type II epithelial cells were removed from adult rat lungs using the modified Dobbs' method. Cell viability was determined by analysis of the total protein content, and from the rate of protein synthesis as indicated by the [35S]methionine uptake assay. The results show that verapamil does not have a direct cytoprotective or cytotoxic effect on the incubated cells, but diltiazem seems to be toxic to the cells, especially during cold ischaemia when the toxicity is significant ( P < 0.05). Thus, the protection from ischaemia previously attributed to calcium channel blockers is ascribed to action on the blood vessels resulting in vasodilatation, rather than to a direct influence on cytosolic free calcium homeostasis.

The Effects of Chloride Channel Blockers on Platelet Cytoplasmic Free Calcium Concentration and Platelet Aggregation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3879-3879
Author(s):  
Songmei Yin ◽  
Xiaolin Chen ◽  
Danian Nie ◽  
Shuangfeng Xie ◽  
Liping Ma ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Chloride Channel ◽  
Calcium Concentration ◽  
Disulfonic Acid ◽  
Free Calcium ◽  
Channel Blockers ◽  
Free Calcium Concentration ◽  
Cytoplasmic Free Calcium

Abstract Objective To explore the effects of chloride channels on the regulations of platelet cytoplasmic free calcium concentration ([Ca2+]i) and platelet aggregation (PAG). Methods Platelet were separated freshly and then activated by thrombin; The chloride channel blockers 4,4′-diisothiocyano-2, 2′-disulfonic acid stilbene (DIDS) or niflumic acid (NFA), and calcium channel blockers 1-{β-[3-(4-methoxyphenyl)propoxy]- 4-methoxyphenethyl}- 1H - imidazole hydrochloride (SK&F96365) or Nifedipine were added to react with the activated platelets. The effects of each agent on platelet [Ca2+]i and PAG were detected. The combine effects and the interactions among chloride channel blockers (DIDS, NFA) and calcium channel blockers (SK&F96365, Nifedipine) were also investigated. Results Both DIDS and NFA [the concentration were12.5, 25, 50, 100 and 200μmol•L−1 respectively] could inhibit the PAG induced by thrombin (1U/ml) and the effect was dose-dependent. Compared with the control, they had no significant effects on resting [Ca2+]i. Compare with the control group, DIDS (100μmol•L−1), SK&F96365 (100μmol•L−1) and Nifedipine (100μmol•L−1) could significantly reduce the PAG, Ca2+ release and Ca2+ influx activated by thrombin in platelet (P<0.05). DIDS (100μmol•L−1) and SK&F96365 (100μmol•L−1) could enhance each other’s effect on reducing the PAG, Ca2+ release and Ca2+ influx (P<0.05). DIDS (100μmol•L−1) and Nifedipine (100μmol•L−1) could enhance each other’s effect on reducing Ca2+ release (P<0.05). NFA (100μmol•L−1) and SK&F96365 (100μmol•L−1) could weaken each other’s effect on Ca2+ release (P<0.05). NFA (100μmol•L−1) and Nifedipine (100μmol•L−1) could weaken each other’s effect on PAG, Ca2+ release and Ca2+ influx activated by thrombin in platelet (P<0.05). Conclusion The chloride channel blockers DIDS and NFA have no effect on the resting [Ca2+]i and the leak calcium influx of platelet. DIDS can inhibit the Ca2+ release, Ca2+ influx and PAG of platelet induced by thrombin, while NFA can only inhibit the Ca2+ release of platelet induced by thrombin. There are interactions between chloride channel blockers and calcium channel blockers in resting [Ca2+]i and PAG of platelet. The opening of chloride channel can influence the cellular calcium movement of platelet.

scholarly journals A Systematic Review on 1, 4-Dihydropyridines and its Analogues: An Elite Scaffold

2021 ◽  
Vol 12 (3) ◽  
pp. 3117-3134
Keyword(s):  
Myocardial Infarction ◽  
Systematic Review ◽  
Clinical Trials ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Channel Blockers ◽  
Neuroprotective Effects ◽  
Dihydropyridine Derivatives

1,4-Dihydropyridines are a group of pyridine-based molecules possessing a magnificent set of biological and therapeutic potentials. Belonging to the class of calcium channel blockers, they are known to be effective in the conditions, angina, hypertension, myocardial infarction and show vasodilatory and cardiac depressant effects. Hypotensive, antimicrobial, anticancer, anticoagulant, antioxidant, anticonvulsant, antimalarial, antiulcer, and neuroprotective effects have been reported with their rational use. The effects are precipitated in response to inhibition of calcium channels, gradually restricting calcium influx. Drugs like nifedipine, felodipine, and amlodipine are commonly used clinically. Several other drugs belonging to this class have been under clinical trials. The present review focuses on the various 1,4-dihydropyridine derivatives and their pharmacological actions.

scholarly journals Calcium channel blockers do not protect against saturated fatty acid-induced ER stress and apoptosis in human pancreatic β-cells

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Jan Šrámek ◽  
Vlasta Němcová ◽  
Jan Kovář
Keyword(s):  
Er Stress ◽  
Calcium Channel ◽  
Cell Lines ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Saturated Fatty Acids ◽  
Channel Blockers ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells

AbstractIt was evidenced that saturated fatty acids (FAs) have a detrimental effect on pancreatic β-cells function and survival, leading to endoplasmic reticulum (ER) calcium release, ER stress, and apoptosis. In the present study, we have tested the effect of three calcium influx inhibitors, i.e., diazoxide, nifedipine, and verapamil, on the apoptosis-inducing effect of saturated stearic acid (SA) in the human pancreatic β-cell lines NES2Y and 1.1B4. We have demonstrated that the application of all three calcium influx inhibitors tested has no inhibitory effect on SA-induced ER stress and apoptosis in both tested cell lines. Moreover, these inhibitors have pro-apoptotic potential per se at higher concentrations. Interestingly, these findings are in contradiction with those obtained with rodent cell lines and islets. Thus our data obtained with human β-cell lines suggest that the prospective usage of calcium channel blockers for prevention and therapy of type 2 diabetes mellitus, developed with the contribution of the saturated FA-induced apoptosis of β-cells, seems rather unlikely.

Inhibition by calcium channel blockers of the glycogenolytic effect of glucagon in perfused rat liver

1982 ◽  
Vol 99 (4) ◽  
pp. 559-566 ◽  
Author(s):  
Satoshi Kimura ◽  
Toshio Matsumoto ◽  
Ryoko Tada ◽  
Etsuro Ogata ◽  
Kaoru Abe
Keyword(s):  
Cyclic Amp ◽  
Calcium Channel ◽  
Rat Liver ◽  
Calcium Channel Blockers ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Channel Blockers ◽  
Perfused Rat Liver ◽  
Glycogenolytic Effect ◽  
Glucose Output

Abstract. Verapamil and diltiazem, calcium channel blockers, inhibited significantly the glucagon-induced glucose output and 45Ca efflux from perfused rat liver at concentrations higher than 50 μm when the perfusate contained calcium. Although the blockers partially interfered with glucagon-induced elevation of cyclic AMP in the tissue, they also inhibited the effects of cyclic AMP. The blockers did not show the inhibitory effects in the absence of perfusate calcium. However, the inhibition of calcium influx into hepatocytes by omission of extracellular calcium or addition of EGTA did not interfere with these effects of glucagon and cyclic AMP. In the presence of extracellular calcium, the blockers did not inhibit cyanide-induced glucose output, indicating that the activity of glycogen phosphorylase and later processes leading to glucose output were not affected by the blockers. These data suggest that, in the presence of calcium, the blockers inhibit the effect of glucagon also at a step (or steps) subsequent to cyclic AMP production and before the activation of phosphorylase b, probably by inhibiting glucagon-induced mobilization of calcium from intracellular calcium pools rather than inhibiting calcium influx into hepatocytes.

Effects of Calcium-Channel Blockers on Cytosolic Free Calcium and Amylase Secretion in Rat Pancreatic Acini

1991 ◽  
Vol 68 (2) ◽  
pp. 83-87 ◽  
Author(s):  
Yoshiyuki Arita ◽  
Toshinari Kimura ◽  
Tsuyoshi Yazu ◽  
Yoshimitsu Ogami ◽  
Hajime Nawata
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Free Calcium ◽  
Amylase Secretion ◽  
Channel Blockers ◽  
Cytosolic Free Calcium ◽  
Pancreatic Acini

scholarly journals Identification of the multidrug resistance-related membrane glycoprotein as an acceptor for calcium channel blockers.

1987 ◽  
Vol 262 (16) ◽  
pp. 7884-7888 ◽  
Author(s):  
A R Safa ◽  
C J Glover ◽  
J L Sewell ◽  
M B Meyers ◽  
J L Biedler ◽  
...  
Keyword(s):  
Multidrug Resistance ◽  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Membrane Glycoprotein ◽  
Channel Blockers

scholarly journals The transmembrane signaling pathway involved in directed movements of Chlamydomonas flagellar membrane glycoproteins involves the dephosphorylation of a 60-kD phosphoprotein that binds to the major flagellar membrane glycoprotein.

1994 ◽  
Vol 127 (3) ◽  
pp. 803-811 ◽  
Author(s):  
R A Bloodgood ◽  
N L Salomonsky
Keyword(s):  
Monoclonal Antibody ◽  
Signaling Pathway ◽  
Live Cells ◽  
Cross Linking ◽  
Carbohydrate Binding ◽  
Membrane Glycoprotein ◽  
Channel Blockers ◽  
Membrane Glycoproteins ◽  
Flagellar Membrane

Cross-linking of Chlamydomonas reinhardtii flagellar membrane glycoproteins results in the directed movements of these glycoproteins within the plane of the flagellar membrane. Three carbohydrate-binding reagents (FMG-1 monoclonal antibody, FMG-3 monoclonal antibody, concanvalin A) that induce flagellar membrane glycoprotein crosslinking and redistribution also induce the specific dephosphorylation of a 60-kD (pI 4.8-5.0) flagellar phosphoprotein (pp60) that is phosphorylated in vivo on serine. Ethanol treatment of live cells induces a similar specific dephosphorylation of pp60. Affinity adsorption of flagellar 32P-labeled membrane-matrix extracts with the FMG-1 monoclonal antibody and concanavalin A demonstrates that pp60 binds to the 350-kD class of flagellar membrane glycoproteins recognized by the FMG-1 monoclonal antibody. In vitro, protein phosphatase 2B (calcineurin) removes 60% of the 32P from pp60; this correlates well with previous observations that directed flagellar glycoprotein movements are dependent on micromolar calcium in the medium and are inhibited by calcium channel blockers and calmodulin antagonists. The data reported here are consistent with the dephosphorylation of pp60 being a step in the signaling pathway that couples flagellar membrane glycoprotein cross-linking to the directed movements of flagellar membrane glycoproteins.

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